Pharmacological functions of salidroside in renal diseases: facts and perspectives

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Abstract

Rhodiola rosea is a valuable functional medicinal plant widely utilized in China and other Asian countries for its anti-fatigue, anti-aging, and altitude sickness prevention properties. Salidroside, a most active constituent derived from Rhodiola rosea, exhibits potent antioxidative, hypoxia-resistant, anti-inflammatory, anticancer, and anti-aging effects that have garnered significant attention. The appreciation of the pharmacological role of salidroside has burgeoned over the last decade, making it a beneficial option for the prevention and treatment of multiple diseases, including atherosclerosis, Alzheimer’s disease, Parkinson’s disease, cardiovascular disease, and more. With its anti-aging and renoprotective effects, in parallel with the inhibition of oxidative stress and inflammation, salidroside holds promise as a potential therapeutic agent for kidney damage. This article provides an overview of the microinflammatory state in kidney disease and discuss the current therapeutic strategies, with a particular focus on highlighting the recent advancements in utilizing salidroside for renal disease. The potential mechanisms of action of salidroside are primarily associated with the regulation of gene and protein expression in glomerular endothelial cells, podocytes, renal tubule cells, renal mesangial cells and renal cell carcinoma cell, including TNF-α, TGF-β, IL-1β, IL-17A, IL-6, MCP-1, Bcl-2, VEGF, ECM protein, caspase-3, HIF-1α, BIM, as well as the modulation of AMPK/SIRT1, Nrf2/HO-1, Sirt1/PGC-1α, ROS/Src/Cav-1, Akt/GSK-3β, TXNIP-NLRP3, ERK1/2, TGF-β1/Smad2/3, PI3K/Akt, Wnt1/Wnt3a β-catenin, TLR4/NF-κB, MAPK, JAK2/STAT3, SIRT1/Nrf2 pathways. To the best of our knowledge, this review is the first to comprehensively cover the protective effects of salidroside on diverse renal diseases, and suggests that salidroside has great potential to be developed as a drug for the prevention and treatment of metabolic syndrome, cardiovascular and cerebrovascular diseases and renal complications.

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Oxidative stress and diabetic complications.

Ferdinando Giacco, Michael Brownlee, Ann Marie Schmidt (2010)

Oxidative stress plays a pivotal role in the development of diabetes complications, both microvascular and cardiovascular. The metabolic abnormalities of diabetes cause mitochondrial superoxide overproduction in endothelial cells of both large and small vessels, as well as in the myocardium. This increased superoxide production causes the activation of 5 major pathways involved in the pathogenesis of complications: polyol pathway flux, increased formation of AGEs (advanced glycation end products), increased expression of the receptor for AGEs and its activating ligands, activation of protein kinase C isoforms, and overactivity of the hexosamine pathway. It also directly inactivates 2 critical antiatherosclerotic enzymes, endothelial nitric oxide synthase and prostacyclin synthase. Through these pathways, increased intracellular reactive oxygen species (ROS) cause defective angiogenesis in response to ischemia, activate a number of proinflammatory pathways, and cause long-lasting epigenetic changes that drive persistent expression of proinflammatory genes after glycemia is normalized ("hyperglycemic memory"). Atherosclerosis and cardiomyopathy in type 2 diabetes are caused in part by pathway-selective insulin resistance, which increases mitochondrial ROS production from free fatty acids and by inactivation of antiatherosclerosis enzymes by ROS. Overexpression of superoxide dismutase in transgenic diabetic mice prevents diabetic retinopathy, nephropathy, and cardiomyopathy. The aim of this review is to highlight advances in understanding the role of metabolite-generated ROS in the development of diabetic complications.

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Ferroptosis is an autophagic cell death process.

Minghui Gao, Prashant Monian, Qiuhui Pan … (2016)

Ferroptosis is an iron-dependent form of regulated necrosis. It is implicated in various human diseases, including ischemic organ damage and cancer. Here, we report the crucial role of autophagy, particularly autophagic degradation of cellular iron storage proteins (a process known as ferritinophagy), in ferroptosis. Using RNAi screening coupled with subsequent genetic analysis, we identified multiple autophagy-related genes as positive regulators of ferroptosis. Ferroptosis induction led to autophagy activation and consequent degradation of ferritin and ferritinophagy cargo receptor NCOA4. Consistently, inhibition of ferritinophagy by blockage of autophagy or knockdown of NCOA4 abrogated the accumulation of ferroptosis-associated cellular labile iron and reactive oxygen species, as well as eventual ferroptotic cell death. Therefore, ferroptosis is an autophagic cell death process, and NCOA4-mediated ferritinophagy supports ferroptosis by controlling cellular iron homeostasis.

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Is Open Access

HIF-1α pathway: role, regulation and intervention for cancer therapy

Georgina Masoud, Wei Li (2015)

Hypoxia-inducible factor-1 (HIF-1) has been recognized as an important cancer drug target. Many recent studies have provided convincing evidences of strong correlation between elevated levels of HIF-1 and tumor metastasis, angiogenesis, poor patient prognosis as well as tumor resistance therapy. It was found that hypoxia (low O2 levels) is a common character in many types of solid tumors. As an adaptive response to hypoxic stress, hypoxic tumor cells activate several survival pathways to carry out their essential biological processes in different ways compared with normal cells. Recent advances in cancer biology at the cellular and molecular levels highlighted the HIF-1α pathway as a crucial survival pathway for which novel strategies of cancer therapy could be developed. However, targeting the HIF-1α pathway has been a challenging but promising progresses have been made in the past twenty years. This review summarizes the role and regulation of the HIF-1α in cancer, and recent therapeutic approaches targeting this important pathway.

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Author and article information

Contributors

Qiong Liu: URI : https://loop.frontiersin.org/people/2142743/overviewRole: Role:

Jianzhu Chen: URI : https://loop.frontiersin.org/people/2591103/overviewRole:

Anqi Zeng: Role: Role: Role: Role:

Linjiang Song: URI : https://loop.frontiersin.org/people/1817739/overview

Journal

Journal ID (nlm-ta): Front Pharmacol

Journal ID (iso-abbrev): Front Pharmacol

Journal ID (publisher-id): Front. Pharmacol.

Title: Frontiers in Pharmacology

Publisher: Frontiers Media S.A.

ISSN (Electronic): 1663-9812

Publication date (Electronic): 08 January 2024

Publication date Collection: 2023

Volume: 14

Electronic Location Identifier: 1309598

Affiliations

[1] ¹ School of Medical and Life Sciences , Chengdu University of Traditional Chinese Medicine , Chengdu, Sichuan, China

[2] ² Translational Chinese Medicine Key Laboratory of Sichuan Province , Sichuan Academy of Chinese Medicine Sciences , Sichuan Institute for Translational Chinese Medicine , Chengdu, Sichuan, China

Author notes

Edited by: Rahul Sharma, University of Virginia, United States

Reviewed by: Xie-An Yu, Shenzhen Institute For Drug Control, China

Diogo B. Peruchetti, Federal University of Minas Gerais, Brazil

*Correspondence: Linjiang Song, songlinjiang@ 123456cdutcm.edu.cn ; Anqi Zeng, zeng6002aq@ 123456163.com

Article

Publisher ID: 1309598

DOI: 10.3389/fphar.2023.1309598

PMC ID: 10800390

PubMed ID: 38259279

SO-VID: e043755f-9d7f-40c4-953e-5987b3117d20

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 08 October 2023

Date accepted : 18 December 2023

Funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The work is supported by Xinglin project of Chengdu University of Traditional Chinese Medicine (ZKYY 2019, MPRC2021012).

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section-at-acceptance Renal Pharmacology

ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine

Keywords: salidroside,diabetic nephropathy,renal interstitial fibrosis,acute kidney injury,inflammation,renal cell carcinoma

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ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine

Keywords: salidroside, diabetic nephropathy, renal interstitial fibrosis, acute kidney injury, inflammation, renal cell carcinoma

Pharmacological functions of salidroside in renal diseases: facts and perspectives

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Karger: Nephrology

Most cited references 188

Oxidative stress and diabetic complications.

Ferroptosis is an autophagic cell death process.

HIF-1α pathway: role, regulation and intervention for cancer therapy

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